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Slow pathway ablation for typical atrioventricular nodal re-entrant tachycardia significantly alters the autonomic modulation of atrioventricular conduction
S. Havranek, L. Souckova, J. Simek, D. Wichterle,
Language English Country Germany
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 2002-02-01 to 2019-01-31
Medline Complete (EBSCOhost)
from 2003-02-01 to 1 year ago
Health & Medicine (ProQuest)
from 2002-02-01 to 2019-01-31
- MeSH
- Tachycardia, Atrioventricular Nodal Reentry physiopathology surgery MeSH
- Autonomic Nervous System physiopathology MeSH
- Electrocardiography MeSH
- Catheter Ablation * MeSH
- Middle Aged MeSH
- Humans MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
PURPOSE: Atrioventricular (AV) conduction turbulence, biphasic dromotropic response of AV node to single ventricular premature contraction (VPC), consists of early shortening and later prolongation of AV conduction intervals due to the direct electrophysiological mechanisms and perturbation in autonomic modulation. We investigated the acute effect of radiofrequency catheter ablation of slow pathway on AV turbulence. METHODS: The electrophysiological study was performed in 18 patients (7 men, mean age 49 ± 15 years) undergoing catheter ablation for AV nodal reentrant tachycardia. The stimulation protocol consisting of series of isolated VPC (coupling interval of 273 ± 23 ms) delivered from right ventricle apex during constant atrial pacing at 100 bpm was performed immediately prior to and 8 ± 4 min after successful slow-pathway ablation. Averaged post-VPCs profiles of AV conduction intervals were analyzed by purpose-written software. The descriptors of AV turbulence, turbulence onset (TOAV), turbulence slope (TSAV), and AV recovery (R AV) were assessed. RESULTS: Slow-pathway ablation suppressed the AV nodal responsiveness to VPC as evidenced by significant reduction of AV turbulence indices: TOAV: -6.4 ± 7.5 % vs. -4.3 ± 6.1 % (p < 0.05); TSAV: 2.0 ± 2.6 ms/RRi vs. 1.0 ± 0.7 ms/RRi (p < 0.05); and R AV: -13.8 ± 7.3 % vs. -6.5 ± 12.7 % (p < 0.05). CONCLUSIONS: Slow-pathway ablation significantly attenuated both vagal and non-autonomic modulation of AV nodal conduction. This effect is likely due to direct thermal injury of AV node associated with the change of properties of AV nodal fast-pathway although specific alteration of peri-AV nodal ganglionated plexi or their neural inputs into the AV node cannot be excluded.
References provided by Crossref.org
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- $a PURPOSE: Atrioventricular (AV) conduction turbulence, biphasic dromotropic response of AV node to single ventricular premature contraction (VPC), consists of early shortening and later prolongation of AV conduction intervals due to the direct electrophysiological mechanisms and perturbation in autonomic modulation. We investigated the acute effect of radiofrequency catheter ablation of slow pathway on AV turbulence. METHODS: The electrophysiological study was performed in 18 patients (7 men, mean age 49 ± 15 years) undergoing catheter ablation for AV nodal reentrant tachycardia. The stimulation protocol consisting of series of isolated VPC (coupling interval of 273 ± 23 ms) delivered from right ventricle apex during constant atrial pacing at 100 bpm was performed immediately prior to and 8 ± 4 min after successful slow-pathway ablation. Averaged post-VPCs profiles of AV conduction intervals were analyzed by purpose-written software. The descriptors of AV turbulence, turbulence onset (TOAV), turbulence slope (TSAV), and AV recovery (R AV) were assessed. RESULTS: Slow-pathway ablation suppressed the AV nodal responsiveness to VPC as evidenced by significant reduction of AV turbulence indices: TOAV: -6.4 ± 7.5 % vs. -4.3 ± 6.1 % (p < 0.05); TSAV: 2.0 ± 2.6 ms/RRi vs. 1.0 ± 0.7 ms/RRi (p < 0.05); and R AV: -13.8 ± 7.3 % vs. -6.5 ± 12.7 % (p < 0.05). CONCLUSIONS: Slow-pathway ablation significantly attenuated both vagal and non-autonomic modulation of AV nodal conduction. This effect is likely due to direct thermal injury of AV node associated with the change of properties of AV nodal fast-pathway although specific alteration of peri-AV nodal ganglionated plexi or their neural inputs into the AV node cannot be excluded.
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